A conventional pacemaker stimulates a patient's heart to maintain regular contractions of the heart thereby promoting blood circulation within the patient. Such stimulation may be prescribed when the patient's heart does not function normally due to, for example, a genetic or acquired condition involving the sinus node or AV conduction system resulting in a symptomatic bardycardia.
In a healthy heart, contractions occur first in the muscles associated with the atrial chambers of the heart, followed by contractions in the muscles associated with the larger ventricular chambers of the heart. In this way, the atria assist in the filling of the ventricular chambers with blood returning from the veins. This increases the end-diastolic volume increasing the stroke volume to enable the ventricles to more efficiently pump blood to the arteries.
Given the interaction of these chambers, efficient operation of the heart is predicated on each of the chambers operating in a proper timing sequence and having contractions that pump a sufficient amount of blood from the chamber. For example, during contraction the right atrium chamber should pump enough blood to optimally “fill” the right ventricle chamber. Moreover, this should occur immediately before the right ventricle begins to contract. In this way, the heart may efficiently pump blood on a repetitive basis.
A healthy heart repetitively contracts in the above described manner in response to the generation and conduction of electrical signals in the heart. These electrical signals are generated in and conducted through the heart during every beat of the heart. A simplified example of these electrical signals follows.
Activity for a given beat begins with the generation of a signal in a sinus node of the heart. This signal causes contraction to begin first in the atria. The signal from the sinus node propagates via a conduction system to an atrioventricular (“A-V”) node. The signal is delayed for a very short period of time (usually less than 200 ms) within the AV node allowing the atria to contract to help to fill the ventricles. The signal then propagates from the A-V node through the bundle of His to the left and right ventricles via a specialized conduction system. Contraction in each ventricle commences in a coordinated manner when the signal “reaches” the respective muscle fibers in the ventricle.
In a diseased or otherwise unhealthy heart, there may be a disruption or abnormality in the generation and/or propagation of these signals. For example, in some patients the atria may generate signals in a sporadic manner or there may be a blockage that prevents the signal from the sinus node from reaching the ventricles in a normal manner. In either of these cases, the atrial-ventricular timing may be compromised resulting in inefficient operation or failure of the heart. In other patients, the activation of the main pumping chamber, the left ventricle, is abnormal compromising the coordination of left ventricular contraction and thus compromising cardiac efficiency.
Under certain circumstances, a pacemaker may compensate for abnormal operation of a heart by pacing (e.g., stimulating) one or more of the atria and/or ventricles. To stimulate the heart, a typical pacemaker generates a series of electrical signals which are applied to the heart via one or more electrodes implanted in the heart (e.g., in ventricular or atrial chambers). These electrical signals cause the heart to contract in much the same way as the native electrical signals discussed above cause the heart to contract.
To provide appropriate timing for the generation of electrical signals, conventional pacemakers may sense signals in the heart. For example, when a heart has a functioning sinus node but has some form of a blockage between the sinus node and the ventricles, a pacemaker may sense electrical signals in the atria to detect when the atria are being activated. The pacemaker may then delay a prescribed period of time after which it applies a stimulus to the ventricles. In this way, the pacemaker may stimulate the ventricles at the appropriate time in an attempt to maintain efficient operation of the heart.
In recent years, it has been recognized that patients with congestive heart failure due to a mechanical problem with the heart muscle may develop a delay in conduction through the left ventricle further compromising overall cardiac function. This is identified on a surface electrocardiogram (ECG) by a widening of the electrical signal from the ventricle (QRS complex) with a pattern known as intraventricular conduction delay (IVCD) or abnormality, the most common of which is left bundle branch block (“LBBB”). In an effort to restore or improve the coordination of the cardiac contraction, two ventricular leads are being utilized, one placed in the right ventricle to stimulate the left ventricular septum and one advanced through the coronary sinus to stimulate the posterior or lateral wall of the left ventricle via a lead located in a cardiac vein. A transthoracic epicardial lead can achieve a similar result. By stimulating both ventricular leads at the same time or in a specified sequence, resynchronization of the left ventricular contraction pattern can be achieved to improve overall cardiac function. Many patients for whom CRT therapy is recommended do not have sinus node dysfunction or AV block.
Many patients with CHF may suffer from a condition known as atrial tachyarrhythmia. This condition may result in sporadic signals being passed through the A-V node which may cause sporadic activation of the ventricles. More importantly, they compromise ventricular filling by compromising the atria's ability to contract in a coordinated manner. As a result, the ventricles may function in a less efficient or ineffective manner in such patients. A standard DDD pacemaker, if it had been implanted for either AV block or sinus node dysfunction, may track these abnormal atrial signals driving the ventricle at a physiologically inappropriate and rapid rate further compromising ventricular function. Automatic mode switch (AMS) algorithms have been developed to recognize the pathologically rapid atrial rates and convert the pacemaker from a tracking to a nontracking mode. In a patient with a CRT stimulation system who does not have a primary need for pacing therapy, development of a pathologic atrial tachyarrhythmia not only forces a loss of AV synchrony and a generally rapid ventricular rate, it also results in the loss of cardiac resynchronization that was the result of the implanted multisite stimulation system.
Pacing techniques have been proposed for managing the implanted device's response to pathologic atrial tachyarrhythmias that have a standard need for pacing therapy. There is a need for more effective techniques for treating patients with atrial tachyarrhythmia who also have congestive heart failure, a disordered ventricular activation sequence associated with intrinsic conduction and in whom multisite ventricular pacing is being utilized in an attempt to restore a left ventricular synchronized contraction pattern. In the presence of standard automatic mode switching algorithms (AMS), switching to a nontracking mode in the presence of an atrial tachyarrhythmia results in the loss of cardiac resynchronization therapy (“CRT”).